Neonatal Death and Heart Failure in Mouse with Transgenic HSP60 Expression

doi:10.1155/2015/539805

CNU IR > Pharmacy and Science > Dept. of Biotechnology (including master's program) > Periodical Articles > Item 310902800/29563

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题名:	Neonatal Death and Heart Failure in Mouse with Transgenic HSP60 Expression
作者:	Chen, Tsung-Hsien Liu, Shan-Wen Chen, Mei-Ru Cho, Kuan-Hung Chen, Tzu-Yin Chu, Pao-Hsien Kao, Yu-Ying Hsu, Ching-Han Lin, Kurt Ming-Chao
贡献者:	生物科技系
关键词:	Shock proteins Molecular chaperones Ischemia/reperfusion injury Apoptosis Heat-shock-protein-60 Stress Cells Hsp10 Mice Overexpression
日期:	2015
上传时间:	2016-04-19 19:00:23 (UTC+8)
出版者:	Hindawi Publishing Corp
摘要:	Mitochondrial heat shock proteins, such as HSP60, are chaperones responsible for the folding, transport, and quality control of mitochondrial matrix proteins and are essential for maintaining life. Both prosurvival and proapoptotic roles have been proposed for HSP60, and HSP60 is reportedly involved in the initiation of autoimmune, metabolic, and cardiovascular diseases. The role of HSP60 in pathogenesis of these diseases remains unclear, partly because of the lack of mouse models expressing HSP60. In this study we generated HSP60 conditional transgenic mice suitable for investigating in vivo outcomes by expressing HSP60 at the targeted organ in disease models. Ubiquitous HSP60 induction in the embryonic stage caused neonatal death in mice at postnatal day 1. A high incidence of atrial septal defects was observed in HSP60-expressing mice, with increased apoptosis and myocyte degeneration that possibly contributed to massive hemorrhage and sponge-like cardiac muscles. Our results showed that neonatal heart failure through HSP60 induction likely involves developmental defects and excessive apoptosis. The conditional HSP60 mouse model is useful for studying crucial biological questions concerning HSP60.
關聯:	Biomed Research International, v.2015, Article ID 539805
显示于类别:	[Dept. of Biotechnology (including master's program)] Periodical Articles

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